Avian Pathogenic (APEC) Strain-Dependent Immunomodulation of Respiratory Granulocytes and Mononuclear Phagocytes in -Reporter Transgenic Chickens.

Avian pathogenic (APEC) cause severe respiratory and systemic disease in chickens, commonly termed colibacillosis. Early immune responses after initial infection are highly important for the outcome of the infection. In this study, the early interactions between -expressing APEC strains of serotypes O1:K1:H7 and O2:K1:H5 and phagocytic cells in the lung of -reporter transgenic chickens were investigated. -reporter transgenic chickens express fluorescent protein under the control of elements of the promoter and enhancer, such that cells of the myeloid lineage can be visualized and sorted. Chickens were separately inoculated with APEC strains expressing and culled 6 h post-infection. Flow cytometric analysis was performed to phenotype and sort the cells that harbored bacteria in the lung, and the response of the sorted cells was defined by transcriptomic analysis. Both APEC strains were mainly detected in -transgene (-tg) and -tg MHC II MRC1L-B cells and low numbers of APEC were detected in -tg MHC II MRC1L-B cells. Transcriptomic and flow cytometric analysis identified the APEC-tg and -tg cells as heterophils and the APEC-tg cells as macrophages and dendritic cells. Both APEC strains induced strong inflammatory responses, however in both -tg and -tg cells, many immune related pathways were repressed to a greater extent or less activated in birds inoculated with APEC O2- compared to APEC O1- inoculated birds. Comparison of the immune pathways revealed the aryl hydrocarbon receptor () pathway, and signaling, heterophil recruitment pathways and the acute phase response, are modulated particularly post-APEC O2- inoculation. In contrast to data, APEC O2- was more invasive in -tg cells than APEC O1- and had higher survival rates for up to 6 h post-infection. Our data indicate significant differences in the responses induced by APEC strains of prevalent serotypes, with important implications for the design and interpretation of future studies. Moreover, we show that bacterial invasion and survival in phagocyte populations is not predictive of events in the chicken lung.